2006 Fiscal Year Final Research Report Summary
Molecular analysis of-defensin on expression and host defense in bronchial cells
| Project/Area Number |
17590799
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | University of Miyazaki |
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Principal Investigator |
ASHITANI Jun-ichi University of Miyazaki, Faculty of Medicine, Associated Professor., 医学部, 助教授 (50347069)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAZATO Masamitsu University of Miyazaki, Faculty of Medicine, Professor., 医学部, 教授 (10180267)
MATSUMOTO Nobuhiro University of Miyazaki, Faculty of Medicine, Assistant., 医学部, 助手 (70418838)
YANAGI Shigehisa University of Miyazaki, Faculty of Medicine, Clinical Fellow., 医学部, 医員 (60404422)
KODAMA Tsuyoshi University of Miyazaki, Faculty of Medicine, Clinical Fellow., 医学部, 医員 (80404424)
KYOURAKU Yuka University of Miyazaki, Faculty of Medicine, Clinical Fellow., 医学部, 医員 (90404425)
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| Project Period (FY) |
2005 – 2006
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| Keywords | respiratory infection / antimicrobial peptide / epithelial lining fluid / defensin |
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| Research Abstract |
This study manly aimed to clarify the significance of β-defensins, antimicrobial peptides localized in respiratory epithelial cells, in respiratory infectious diseases using a molecular biological technique. During recent two years, the following results were obtained using the techniques that had been already established: 1) By using a high sensitivity radioimmunoassay method for β defensins-4, the concentrations of blood and epithelial lining fluid in patients with respiratory infections in the acute and recovery phase were measured; 2) Local expression of β defensins-4 was investigated by immunohistochemical method; 3) The addition of lipopolysaccharide was found to induce the expression of β defensins-4 from cultured bronchial epithelial cells; 4) The differences in the expression of β defensins in respiratory epithelial lining fluid between mucoid and non-mucoid type P. aeruginosa were determined; 5) The combination of β defensins-subtype strengthened the antibacterial activity against P aeruginosa; and 6) Particularly, the e significance of antibacterial activity of β defensins-2 and-4 was found in mucoid type P aeruginosa infection. The findings of the study have illustrated the significance in the pathophysiology of pulmonary diseases and have provided information on the usefulness of β defensin as a tool of treatment for refractory respiratory infections. As a result, 6 papers that presented the achievements of our studies have been published in major American and European Journals in two years.
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